Figure 2. Decreased acetylation of histone H3 at the mGlu2 promoter in prefrontal cortex of treated, but not untreated, schizophrenic subjects.

(a,b) Digested chromatin was immunoprecipitated with antibody recognizing acetyl-histone H3 (H3ac), and the level of association of the 5HT2A, 5HT2C, mGlu2, or mGlu3 promoters was measured by qPCR. The promoter of β₂-microglobulin (B2M) was included as internal control. Experiments were performed in frontal cortex of untreated schizophrenic subjects and matched controls (a), and in frontal cortex of atypical antipsychotic-treated schizophrenic subjects and matched controls (b). H3ac at mGlu2 promoter in treated schizophrenics: t = 3.96. The α value was corrected for multiple independent null hypotheses by using the Holm’s sequentially rejective Bonferroni method. *P < 0.011; two-tailed Student’s t-test. Error bars represent s.e.m. (c,d) Individual representation of histone H3 acetylation at the mGlu2 promoter in postmortem frontal cortex of untreated schizophrenic subjects and matched controls (c), and in postmortem frontal cortex of atypical antipsychotic-treated schizophrenic subjects and matched controls (d). Results are shown as enrichment values (bound/input). Each datapoint of schizophrenic subject is connected to the datapoint of the respective matched control.